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Disruption of Membranous Monolayers of Cultured Pig and Rat Brain Endothelial Cells Induced by Activated Human Polymorphonuclear Leukocytes

  • Minoru Tomita
  • Yasuo Fukuuchi
  • Norio Tanahashi
  • Masahiro Kobari
  • Hidetaka Takeda
  • Masako Yokoyama
  • Helena Haapaniemi
Part of the Advances in Behavioral Biology book series (ABBI, volume 46)

Summary

Employing VEC-DIC microscopy, we observed in an in vitro system that polymorphonuclear leukocytes (PMNLs) interacted with cultured endothelial cells (ECs) through the following steps:
  1. 1.

    the PMNL flowed in a round shape in the superfusion fluid;

     
  2. 2.

    the PMNL rolled on the EC for a couple of minutes;

     
  3. 3.

    the PMNL remained at a nonspecific location on the plasmic membrane of the EC for a few minutes;

     
  4. 4.

    the PMNL became firmly stuck through connections which were single-stemmed, multichanneled, or en face;

     
  5. 5.

    the PMNL apparently interacted with the EC, causing its retraction and detachment from the floor; and

     
  6. 6.

    finally, the PMNL swelled up in some but not all cases, being hugged by the “dead” EC, which had fallen into coagulation necrosis.

     

Based on these observations, it is speculated that during the above process involving PMNLs, EC damage and shrinkage would cause cracks in the EC layer in the in situ microvessels, not only resulting in fluid leakage from the blood to the tissue, but also providing a gap for the diapedesis of newly arriving white cells, since PMNLs are always available in the blood stream even in ischemic tissue (Fig. 5).

Keywords

Coagulative Necrosis Brain Microvascular Endothelial Cell Observation Chamber Leukocytic Infiltration Phonuclear Leukocyte 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Résumé

Nous avons observé, en microscopie VEC-DIC, dans un système in vitro,que les leucocytes polymorphonucléaires (PMNL) interagissent sur les cellules endotheliales (EC) selon les processus suivants:
  1. 1.

    les PMNL prennent une forme sphérique dans le liquide de perfusion;

     
  2. 2.

    les PMNL roulent sur les EC pendant 2 minutes;

     
  3. 3.

    les PMNL demeurent sur la membrane plasmique des EC, dans un site non spécifique pendant quelques minutes;

     
  4. 4.

    les PMNL s’accolent fermement par des liaisons comportant un seul brin, plusieurs canaux, ou “en face”;

     
  5. 5.

    les PMNL semblent agir sur les Ec, qui se rétractent et se décollent du support;

     
  6. 6.

    et, finalement, les PMNL sont souvent gonflés par les EC “morts” qui les enserrent et qui sont entrés en nécrose et coagulation.

     

Sur la base de ces observations, on suppose que pendant le processus décrit ci-dessus avec les PMNL, la rétraction des EC provoquerait des éclatements in situ dans les couches de EC des microvaisseaux, ce qui induirait non seulement une fuite de fluide du sang vers les tissus, mais ouvrirait aussi une brèche pour la diapédèse de nouvelles cellules blanches, puisque les PMNL sont toujours présents dans le flux sanguin, même dans les tissus ischémies (Fig.5).

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Copyright information

© Springer Science+Business Media New York 1996

Authors and Affiliations

  • Minoru Tomita
    • 1
  • Yasuo Fukuuchi
    • 1
  • Norio Tanahashi
    • 1
  • Masahiro Kobari
    • 1
  • Hidetaka Takeda
    • 1
  • Masako Yokoyama
    • 1
  • Helena Haapaniemi
    • 2
  1. 1.Department of Neurology School of MedicineKeio UniversityTokyoJapan
  2. 2.Department of NeurologyUniversity of HelsinkiFinland

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